114497-66-4

Upstream product

• 14191-95-8 4-cyanomethylphenol 
• 3747-74-8 2-(chloromethyl)quinoline monohydrochloride 
• 4377-41-7 2-Chloromethylquinoline 
• 7757-82-6 sodium sulfate 

Downstream Products

• 107813-83-2 5-[4-(2-quinolylmethyloxy)benzyl]tetrazole 

Relevant academic research and scientific papers

Quinolylmethoxyphenylacetic acid acylamides and ureas

Quinolylmethoxyphenylacetic acid acylamides and ureas can be prepared either by reacting corresponding carboxylic acids with amides or reacting corresponding amides with isocyanates or ureas. The quinolylmethoxyphenylacetic acid acylamides or ureas can be

Quinolylmethoxyphenyl-acetamides

Quinolylmethoxyphenyl-acetamides of the formula: STR1 in which A, B, D, E, G, L and M are hydrogen, hydroxyl, halogen, cyano, carboxyl, nitro, trifluoromethyl, trifluoromethoxy, alkyl, alkoxy or optionally substituted aryl; R1 represents option

Development of a novel series of (2-quinolinylmethoxy)phenyl-containing compounds as high-affinity leukotriene receptor antagonists. 1. Initial structure-activity relationships

This series of reports describes the development of orally active, highly potent, specific antagonists of the peptidoleukotrienes containing a (2-quinolinylmethoxy)phenyl moiety. Described in this first report are the structure-activity relationships that led to more than a 20-fold improvement of the potency and selectivity of the initial chemical lead (RG 5901). From this series of compounds, RG 7152 (16) was identified and selected for further evaluation in the clinic as an antiasthmatic agent. Compound 16 competitively inhibits [3H]LTD4 binding to membranes from guinea pigs lung (K(i) = 38 ± 6 nM) and the spasmogenic activity of LTC4, LTD4, and LTE4 in parenchymal lung strips from guinea pigs. Unlike the original lead (RG 5901), compound 16 does not inhibit 5-lipoxygenase from guinea pig PMNs. Following oral administration to guinea pigs, 16 blocks LTD4-induced dermal permeability (ED50 = 6.9 mg/kg), LTD4-induced bronchoconstriction (ED50 = 1.1 mg/kg), antigen-induced bronchoconstriction (ED50 = 2.5 mg/kg), and anaphylactic-induced mortality (ED50 = 16 mg/kg). These studies on structure-activity relationships indicate that there is a requirement for an acidic function and the presence of the (2-quinolinylmethoxy)phenyl moiety in a specific geometric arrangement.

N- Carboxylic Acids, Hydroxamic Acids, Tetrazoles, and Sulfonyl Carboxamides. Potent Orally Active Leukotriene D4 Antagonists of Novel Structure

Four series of N- compounds were prepared as leukotriene D4 (LTD4) antagonists.In the hydroxamic acid series, methyl 3-(2-quinolinylmethoxy)benzeneacetohydroxamate (Wy-48,422, 20) was the most potent inhibitor of LTD4-induced bronchoconstriction with an oral ED50 of 7.9 mg/kg.Compound 20 was also orally inhibited ovalbumin-induced bronchoconstriction in the guinea pig with an ED50 of 3.6 mg/kg.In vitro, against LTD4-induced contraction of isolated guinea pig trachea pretreated with indomethacin and 1-cysteine, 20 produced a pKB value of 6.08.In the sulfonyl carboxamide series, N--3-(2-quinolinylmethoxy)-benzamide (Wy-49,353, 30) was the most potent antagonist.Compound 30 orally inhibited both LTD4- and ovalbumin-induced bronchoconstriction with ED50s of 0.4 and 20.2 mg/kg, respectively.In vitro, against LTD4-induced contraction of isolated guinea pig trachea, 30 produced a pKB value of 7.78.In the carboxylic acid series, which served as intermediates for the above two series, 3-(2-quinolinylmethoxy)benzeneacetic acid (Wy-46,016, 5) was the most potent inhibitor of LTD4-induced bronchoconstriction (99percent at 25 mg/kg, intraduodenally); however, the pKB for this compound was disappointing (5.79).In the tetrazole series, the most potent inhibitor was 2-methyl>quinoline (Wy-49,451, 41).The respective inhibitory ED50s were 3.0 mg/kg versus LTD4 and 17.5 mg/kg versus ovalbumin.In the isolated guinea pig trachea, 41 produced a pKB value of 6.70.